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Cancer Caused by Diesel Fuel Exhaust Emissions
Published in Ozcan Konur, Petrodiesel Fuels, 2021
Hiura et al. (2000) study the role of a mitochondrial pathway in the induction of apoptosis by chemicals extracted from DEPs in a paper with 158 citations. They showed that methanol extracts made from DEPs induce apoptosis and ‘reactive oxygen species’ (ROS) in pulmonary alveolar macrophages and RAW 264.7 cells. The toxicity of these organic extracts mimics the cytotoxicity of the intact particles and could be suppressed by the synthetic sulfhydryl compounds, ‘N-acetylcysteine’ (NAC) and bucillamine. Because DEP-induced apoptosis follows cytochrome c release, they examined the effect of DEP chemicals on mitochondrially regulated death mechanisms. They found that crude DEP extracts induced ROS production and perturbed mitochondrial function before and at the onset of apoptosis. This mitochondrial perturbation follows an orderly sequence of events, which commence with a change in mitochondrial membrane potential, followed by cytochrome c release, development of membrane asymmetry, and propidium iodide uptake. Structural damage to the mitochondrial inner membrane, evidenced by a decrease in cardiolipin mass, leads to O2 generation and uncoupling of oxidative phosphorylation. NAC reversed these mitochondrial effects and ROS production. Overexpression of the mitochondrial apoptosis regulator, ‘B-cell lymphoma 2’ (Bcl-2), delayed but did not suppress apoptosis. They conclude that DEP chemicals induce apoptosis in macrophages via a toxic effect on mitochondria.
Organic Chemicals
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Peroxynitrite, superoxide, and their products lead to lipid peroxidation of the cardiolipin in the inner membrane of the mitochondrion. Cardiolipin is highly susceptible to such peroxidation because most of the fatty acids that make up its structure in mammals are polyunsaturated fatty acids, which are much more susceptible to peroxidation than are other fatty acids.
27-Deoxyactein prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced cellular damage in MC3T3-E1 osteoblastic cells
Published in Journal of Environmental Science and Health, Part A, 2018
Kwang Sik Suh, Eun Mi Choi, Woon-Won Jung, So Young Park, Sang Ouk Chin, Sang Youl Rhee, Youngmi Kim Pak, Suk Chon
Cardiolipin oxidation induces the opening of permeability pores in the outer mitochondrial membrane, which permits the release of cytochrome c and other pro-apoptotic factors from the mitochondria into the cytosol. Subsequently, cytochrome c release triggers a cascade of caspase interactions that leads to apoptosis.[35] Cardiolipin exists in association with cytochrome c on the outer surface of the inner mitochondrial membrane. Thus, to obtain further evidence of oxidative stress within the mitochondria, the oxidation of cardiolipin was assessed. Because the fluorescent dye NAO binds to the non-oxidized form but not the oxidized form of cardiolipin,[36] measurements of NAO fluorescence allow for the monitoring of the oxidation of cardiolipin in mitochondria. In the present study, treatment with 100 nM of TCDD decreased NAO fluorescence, indicating that cardiolipin peroxidation was induced (Fig. 5). However, 27-deoxyactein (0.01–1 μM) reduced the level of TCDD-induced cardiolipin peroxidation, which suggests that 27-deoxyactein reduced ROS generation and oxidative stress within the mitochondria that were induced by TCDD.
Apigenin attenuates tetrabromobisphenol A-induced cytotoxicity in neuronal SK-N-MC cells
Published in Journal of Environmental Science and Health, Part A, 2023
Eun Mi Choi, So Young Park, Kwang Sik Suh, Suk Chon
To obtain further evidence for oxidative stress within mitochondria, we assessed the oxidation of cardiolipin since this phospholipid exists in association with cytochrome c on the outer surface of the inner mitochondrial membrane. Because the fluorescent dye NAO binds to the non-oxidized form and not to the oxidized form of cardiolipin,[31] measurements of NAO fluorescence allow us to monitor the oxidation of cardiolipin in mitochondria. Treatment with 20 μM TBBPA decreased NAO fluorescence, indicating the induction of cardiolipin peroxidation (Fig. 5D). However, apigenin (1 μM) reduced TBBPA-induced cardiolipin peroxidation. These data show that apigenin reduces TBBPA-induced ROS generation and oxidative stress in the mitochondria.